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Mechanistically, accelerated p53 ubiquitination-mediated degradation and reduced p53 activity result in a decrease in target molecules cyclin-dependent kinase inhibitor p21 and apoptosis regulator Bax levels, and an increase in Cyclin-dependent kinase 1 (CDK1) level, thereby accelerating the G2/M phase transition, inhibiting apoptosis and promoting spermatogonial proliferation (36)

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